Development of Primary Hypothyroidism with the Appearance of Blocking-Type Antibody to Thyrotropin Receptor in Graves' Disease in Late Pregnancy

Thyroid ◽  
1999 ◽  
Vol 9 (2) ◽  
pp. 179-182 ◽  
Author(s):  
YOSHIHIKO UETA ◽  
HIROKO FUKUI ◽  
HIROSHI MURAKAMI ◽  
YUMI YAMANOUCHI ◽  
REI YAMAMOTO ◽  
...  
Keyword(s):  
Late Pregnancy ◽  
Primary Hypothyroidism ◽  
Graves Disease ◽  
Thyrotropin Receptor ◽  
Blocking Type

Eye Signs of Graves' Disease and Blocking-Type Thyrotropin Receptor Autoantibodies

Thyroid ◽  
2006 ◽  
Vol 16 (1) ◽  
pp. 97-98 ◽  
Author(s):  
B. Rees Smith ◽  
P. Nordmeyer ◽  
J. Sanders ◽  
J. Furmaniak
Keyword(s):  
Graves Disease ◽  
Thyrotropin Receptor ◽  
Blocking Type

scholarly journals No Increase of Blocking Type Anti-Thyrotropin Receptor Antibodies During Pregnancy in Patients with Graves’ Disease

2003 ◽  
Vol 88 (12) ◽  
pp. 5871-5874 ◽  
Author(s):  
Nobuyuki Amino ◽  
Yukiko Izumi ◽  
Yoh Hidaka ◽  
Keiko Takeoka ◽  
Yukiko Nakata ◽  
...  
Keyword(s):  
Graves Disease ◽  
Thyrotropin Receptor ◽  
Thyrotropin Receptor Antibodies ◽  
Receptor Antibodies ◽  
Blocking Type

Primary hypothyroidism followed by hyperthyroidism Five case reports

1984 ◽  
Vol 105 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Ståle Skare ◽  
Harald M. M. Frey ◽  
Ragnvald Konow-Thorsen
Keyword(s):  
Case Reports ◽  
Primary Hypothyroidism ◽  
Graves Disease

Abstract. Five patients are described, who developed primary hypothyroidism between 25 and 57 years of age. They were all adequately treated with l-thyroxine. Graves' disease developed six months to 34 years later. Two had TSH binding inhibiting immunoglobulin (TBII) in their serum at this stage. All were treated with carbimazole, and 3 have experienced relapse upon withdrawal. Our patients are discussed in relation to the 16 cases previously reported. The pathogenesis of this condition is open to speculation.

scholarly journals Binding of Human Thyrotropin Receptor Peptides to a Graves’ Disease-Predisposing Human Leukocyte Antigen Class II Molecule

2000 ◽  
Vol 85 (3) ◽  
pp. 1176-1179 ◽  
Author(s):  
Yoshikuni Sawai ◽  
Leslie J. DeGroot
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Class Ii ◽  
Hla Class Ii ◽  
Graves Disease ◽  
T Cell Repertoire ◽  
Thyrotropin Receptor ◽  
Cell Repertoire ◽  
Peptide Epitopes ◽  
Leukocyte Antigen

Abstract Abstract There are many reports that Graves’ disease (GD) is associated with certain human leukocyte antigen (HLA) molecules, in particular DR3. Here we examined the characteristics of binding of human TSH receptor (TSHR) peptides to this disease-associated HLA class II molecule. DR3 molecules bind TSHR immuonodominant peptide epitopes with intermediate affinity. On the contrary, DR3 binds nonimmunogenic peptides either with poor affinity or not at all, with one exceptional peptide that has extremely high affinity. These results suggest that susceptibility to GD associated with inheritance of a specific HLA class II gene is due to the influence of the HLA molecule-TSHR peptide complex on the T cell repertoire.

scholarly journals Pathogenetic Role of Thyrotropin Receptor Antibody in the Development of Hyperthyroidism Following Primary Hypothyroidism

1989 ◽  
Vol 4 (2) ◽  
pp. 118-125 ◽  
Author(s):  
Young Kee Shong ◽  
Bo Youn Cho ◽  
Sung Kwan Hong ◽  
Hong Kyu Lee ◽  
Chang Soon Koh ◽  
...  
Keyword(s):  
Primary Hypothyroidism ◽  
Thyrotropin Receptor ◽  
Pathogenetic Role ◽  
Receptor Antibody ◽  
Thyrotropin Receptor Antibody

scholarly journals Preserved activation of thyrotropin receptor antibody to stimulate thyroid function despite long-term treatment in euthyroid patients with Graves' disease

1998 ◽  
pp. 281-285 ◽  
Author(s):  
M Akuzawa ◽  
M Murakami ◽  
M Yamada ◽  
T Satoh ◽  
H Shimizu ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Normal Subjects ◽  
Term Treatment ◽  
Graves Disease ◽  
Thyrotropin Receptor ◽  
Receptor Antibody ◽  
Thyrotropin Receptor Antibody ◽  
Long Term Treatment ◽  
Tsh Levels

Clinical evaluation was conducted to ascertain whether thyrotropin receptor antibody (TRAb) in the normal range may still be involved in the regulation of thyroid function after prolonged treatment for Graves' disease. All patients (n = 33) were treated with antithyroid drugs for an average of 10.6 years and were under euthyroid conditions in which normal blood levels of tri-iodothyronine (T3) were significantly correlated with blood thyrotropin (TSH) levels, but not with titers of TRAb. A significant correlation was observed between TRAb titer and thyroid-stimulating antibody (TSAb) activity. In contrast, this correlation was not found in normal subjects. After administration of T3 (75 microg daily for 8 days), the patients showed increased levels of T3 with concomitant suppression of TSH levels. Under these conditions, linear regression analysis showed significant correlations of TRAb titer and TSAb activity with 24-h thyroid radioiodine uptake (r = 0.641 and 0.621 respectively, P < 0.01), in contrast to declining blood thyroxine levels. Moreover, the immunoglobulin G (IgG) of the patients precipitated to a greater extent than IgG from normal subjects a peptide consisting of the amino acid sequence near the terminus of the human TSH receptor. These findings indicated that TRAb at normal levels possessed significant unremitting activities on thyroid function despite long-term treatment in euthyroid patients with Graves' disease.

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